scholarly journals Acute and prolonged hindlimb exercise elicits different gene expression in motoneurons than sensory neurons after spinal cord injury

2012 ◽  
Vol 1438 ◽  
pp. 8-21 ◽  
Author(s):  
Benjamin E. Keeler ◽  
Gang Liu ◽  
Rachel N. Siegfried ◽  
Victoria Zhukareva ◽  
Marion Murray ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Sensory Neurons ◽  
Cord Injury

scholarly journals Transcriptional profiling of non-injured nociceptors after spinal cord injury reveals diverse molecular changes

2019 ◽  
Author(s):  
Jessica R. Yasko ◽  
Isaac L. Moss ◽  
Richard E. Mains
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Chronic Pain ◽  
Signaling Pathways ◽  
Sensory Neurons ◽  
Traumatic Spinal Cord Injury ◽  
Post Injury ◽  
Inflammatory Signaling ◽  
Cord Injury

AbstractTraumatic spinal cord injury (SCI) has devastating implications for patients, including a high predisposition for developing chronic pain distal to the site of injury. Chronic pain develops weeks to months after injury, consequently patients are treated after irreparable changes have occurred. Nociceptors are central to chronic pain; however, the diversity of this cellular population presents challenges to understanding mechanisms and attributing pain modalities to specific cell types. To begin to address how peripheral sensory neurons distal to the site of injury may contribute to the below-level pain reported by SCI patients, we examined SCI-induced changes in gene expression in lumbar dorsal root ganglia (DRG) below the site of injury. SCI was performed at the T10 vertebral level, with injury produced by a vessel clip with a closing pressure of 15g for 1 minute. Alterations in gene expression produce long-term sensory changes, therefore we were interested in studying SCI-induced transcripts before the onset of chronic pain, which may trigger changes in downstream signaling pathways and ultimately facilitate the transmission of pain. To examine changes in the nociceptor subpopulation in DRG distal to the site of injury, we retrograde labeled sensory neurons projecting to the hairy hindpaw skin with fluorescent dye and collected the corresponding lumbar (L2-L6) DRG 4 days post-injury. Following dissociation, labeled neurons were purified by fluorescence-activated cell sorting. RNA was extracted from sorted sensory neurons of naïve, sham, or SCI mice and sequenced. Transcript abundances validated that the desired population of nociceptors were isolated. Cross-comparisons to data sets from similar studies confirmed we were able to isolate our cells of interest and identify a unique pattern of gene expression within a subpopulation of neurons projecting to the hairy hindpaw skin. Differential gene expression analysis showed high expression levels and significant transcript changes 4 days post-injury in SCI cell populations relevant to the onset of chronic pain. Regulatory interrelationships predicted by pathway analysis implicated changes within the synaptogenesis signaling pathway as well as networks related to inflammatory signaling mechanisms, suggesting a role for synaptic plasticity and a correlation with pro-inflammatory signaling in the transition from acute to chronic pain.Contribution to the fieldTraumatic spinal cord injury (SCI) has devastating implications for patients, including a high predisposition for developing chronic pain. Much of the pain seems to emanate from tissues further away from the brain than the site of injury. Chronic pain develops weeks to months after injury, which means that patients are frequently treated only after enduring pain has developed. Nociceptors are the specialized sensory neurons central to chronic pain. We were interested in studying SCI-induced gene transcript (RNA) changes before the onset of chronic pain, in the hope of identifying mechanisms which could become therapeutic targets. Nociceptors below the site of spinal injury were isolated and their RNAs were sequenced. The results identified a unique pattern of gene expression in the subpopulation of nociceptors projecting to the relevant peripheral tissue. Particularly interesting were sets of genes crucial to synapse formation and maturation – the ability of neurons to talk to each other – and genes involved in inflammatory responses, since treatment of inflammation of nervous tissue could also be important for therapeutic approaches. It is evident that the transition from acute to chronic pain occurs in distinct steps that involve numerous signaling pathways, providing a host of potential new drug targets.

233-LB: Spinal Cord Injury Inhibited-FGF21 Signaling Is Associated with Dysregulation of Metabolic Gene Expression in Mouse Liver and Adipose Tissue

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 233-LB
Author(s):  
XIN-HUA LIU ◽  
LAUREN HARLOW ◽  
ZACHARY GRAHAM ◽  
JOSHUA F. YARROW ◽  
KENNETH CUSI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adipose Tissue ◽  
Mouse Liver ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury

scholarly journals Plasticity of TRPV1-Expressing Sensory Neurons Mediating Autonomic Dysreflexia Following Spinal Cord Injury

2012 ◽  
Vol 3 ◽  
Author(s):  
Leanne M. Ramer ◽  
A. Peter van Stolk ◽  
Jessica A. Inskip ◽  
Matt S. Ramer ◽  
Andrei V. Krassioukov
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Sensory Neurons ◽  
Autonomic Dysreflexia ◽  
Cord Injury

scholarly journals The effect of spinal cord injury on the neurochemical properties of vagal sensory neurons

2015 ◽  
Vol 308 (12) ◽  
pp. R1021-R1033 ◽  
Author(s):  
April N. Herrity ◽  
Jeffrey C. Petruska ◽  
David P. Stirling ◽  
Kristofer K. Rau ◽  
Charles H. Hubscher
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Vagus Nerve ◽  
Sensory Neurons ◽  
Receptor Expression ◽  
Vagal Afferents ◽  
Cord Injury ◽  
Male Wistar Rats ◽  
Neurochemical Plasticity ◽  
Isolectin B4

The vagus nerve is composed primarily of nonmyelinated sensory neurons whose cell bodies are located in the nodose ganglion (NG). The vagus has widespread projections that supply most visceral organs, including the bladder. Because of its nonspinal route, the vagus nerve itself is not directly damaged from spinal cord injury (SCI). Because most viscera, including bladder, are dually innervated by spinal and vagal sensory neurons, an impact of SCI on the sensory component of vagal circuitry may contribute to post-SCI visceral pathologies. To determine whether SCI, in male Wistar rats, might impact neurochemical characteristics of NG neurons, immunohistochemical assessments were performed for P2X3 receptor expression, isolectin B4 (IB4) binding, and substance P expression, three known injury-responsive markers in sensory neuronal subpopulations. In addition to examining the overall population of NG neurons, those innervating the urinary bladder also were assessed separately. All three of the molecular markers were represented in the NG from noninjured animals, with the majority of the neurons binding IB4. In the chronically injured rats, there was a significant increase in the number of NG neurons expressing P2X3 and a significant decrease in the number binding IB4 compared with noninjured animals, a finding that held true also for the bladder-innervating population. Overall, these results indicate that vagal afferents, including those innervating the bladder, display neurochemical plasticity post-SCI that may have implications for visceral homeostatic mechanisms and nociceptive signaling.

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